"A New Concept in the Treatment of Obesity"
JAMA 1963 Oct 5 , pp. 156-163 , Vol. 186, No. 1
Edgar S. Gordon MD, Marshall Goldberg MD, Grace J. Chosy, BS
(2008 Jan blog post)
Many critics of Dr. Atkins and his lowered-carbs diet seem to think he pulled his diet out of thin air. They seem to lack the will to look up the texts that he credits with leading to his diet proposals.
(Ironically, many of his strongest critics are doctors in the AMA, American Medical Association --- and Atkins got his inspiration from papers published in the JAMA, Journal of the American Medical Association. Further irony: Those papers were written by doctors who were members of the AMA --- and were reviewed and accepted for publication by doctors in the AMA.)
His diet (actually, a lifetime-way-of-eating methodology) was not invented by him. He was actually trying to popularize medical study results that he had read about in medical journal articles published back in the early 1960's --- for the benefit of his patients, for the citizens of this country, and for the citizens of the world.
In other words, he was trying to communicate important health information that was "locked away" in stuffy old medical journals, in and among pages of mind-numbing verbiage.
To quote Atkins in his book "Atkins for Life", 2003, page xii:
"The first published documentation of the success of a controlled carbohydrate dietary regimen appeared in the 1800s, but we needn't go back that far. It was after reading a scientific study [its text is below] on the effectiveness of several low carbohydrate weight-loss programs in the October 1963 issue of the Journal of the American Medical Association [JAMA] that I decided to put a similar approach into practice.
We now have, on our web site www.atkinscenter.com, summaries of close to four hundred [ 400 ! ] scientific studies that support the principles upon which the controlled carbohydrate nutritional approach is based."
And in the back of the book "The Atkins Essentials" (2004) that was published after Atkins' death, there is a bibliography of 15 peer-reviewed studies, published in 2001 to 2003, that specifically focused on the outcomes that result from the "Atkins Nutritional Approach".
Many of these recent studies come from respected researchers at institutions such as Harvard and Stanford --- again, members of the AMA. I find it amazing that people (many of them doctors and dieticians) who debunk lowered-carbs diets can simply ignore these studies, or pass them off as invalid.
Simplification of the Atkins diet
For many, it would be extremely difficult to follow a dietary regimen as strictly as the regimen documented in clinical studies. If you don't like to try to keep track of the ratio of protein-to-fat-to-carbs that you are eating (I sure don't) --- and if you don't like to to count grams or calories (I sure don't), then, as a simpler alternative, just try the 'No Flour, No Sugar Diet' proposed by Dr. Gott M.D. in a book by that name. He realizes that it is just too much to expect that people can and will do those diet-math things --- especially on a day-to-day basis.
(By the way, Dr. Gott, I would guess, is a member of the AMA --- unless he has been driven out by anti-lowcarb-diet doctors high up in the AMA hierarchy. His "lowered-carbs"-views, and, especially, the publishing of those views for the world to see, must have made him the target of powerful 'sugar-and-starch carbohydrate interests'.)
(I have to wonder what is driving those anti-lowcarb-diet AMA doctors to 'bad mouth' Atkins so vehemently --- monetary ties to soft-drink/candy/processed-foods/drug/insulin industries?)
Source of the Atkins-inspiring medical reports
The majority of the text of the "scientific study" mentioned in the Atkins quote above is presented below. This is the study that led to his many years spent in formulating and promoting a lowered-carbs way of eating, to help many of his patients --- and ultimately anyone who was in need of help and who would listen.
I could no longer find the Oct 1963 article on-line on the internet. Even the JAMA web site does not have journal articles on-line that the JAMA published before the mid-1960's. So I found the article in a university medical school library --- and I have devoted some hours to keying in the major part of the text, so that the article is preserved on-line.
NOTE: I have added bold font to some statements of the report that seemed especially important to me, based on my experiences. And I have inserted some notes. Those notes are enclosed in brackets.
In finding that Oct 1963 JAMA article, I ran across a Dec 1963 JAMA article that Atkins probably saw. The Dec 1963 article takes a more "clinical-data-only" approach, than the Oct 1963 article, in pointing out the benefits of a lowered-carbs diet. The results come from a "dietetic outpatient clinic" --- and the paper says right-out in the introductory summary that patients "came to eat a low-carbohydrate, high-protein diet". That probably caught Atkins' eye --- along with the term "obesity" in the title.
Since that article probably erased any doubts that Atkins may have had about the likelihood of success in trying a lowered-carbs way of eating, I have keyed in a majority of the text of that Dec 1963 article. The text is available via this "hyper-link".
Read the Oct and Dec 1963 texts yourself. See if you would have come to the same course of action that Atkins pursued, if you had a medical practice like he had.
Note that this Oct 1963 paper starts the diet with a 48-hour fast --- to break previous patterns of dietary behavior. The Atkins diet starts with a milder form of this --- an "induction" phase.
Start of the paper :
A New Concept in the Treatment of Obesity
Edgar S. Gordon MD, Marshall Goldberg MD, Grace J. Chosy, BS
JAMA Vol. 186, No. 1, pp. 156-166, 1963 Oct 5
From the departments of medicine and dietetics,
Accordingly, about 3 years ago, detailed studies of obese subjects were undertaken with the basic objective of ascertaining if their patterns of energy metabolism are significantly different from those of normal control subjects. These efforts were facilitated by an impressive and growing fund of basic information in this field that has accumulated especially during the last 10 years, and by the availability of numerous elegant new biochemical research techniques that had never been applied to the investigation of this clinical problem. It became apparent very early in these studies that a number of metabolic anomalies could be demonstrated, each one representing a biochemical or physiological measurement in which the obese subjects behaved quite differently from normal control subjects.
The magnitudes of these differences have been found to vary widely from one subject to another, so that the abnormalities that characterize this condition [obesity] may not be regarded as all or none, black or white, but constitute, instead a continuum of varying shades of gray extending from extreme abnormality to completely normal.
A list of these abnormal findings is presented in this report [a couple of paragraphs below]. It should be emphasized that marked variation may be seen from one individual to another so that many of these anomalies may be present in only a limited number of patients. Of particular interest is the group designated as "resistant obese". These people always have presented a difficult and perplexing problem of management to physicians.
Since these findings represent the contributions of many laboratories documentation is provided in the references as designated.
[NOTE: To make this paper more readable to non-medical-researchers and to avoid obfuscating the basic dietary issues that are the main subject of this paper, some items in the list are not presented. I show those items that would have meaning to the average reader and to people, such runners and dieters, who would be familiar with such terms as glucose, insulin, triglycerides, free-fatty-acids, and lactate. Or, in the authors own words, see the following statements.]
It is not within the scope of this report to discuss each of these findings in detail, since they will appear as research reports in separate publications. Furthermore, some of these findings are not yet well enough documented by clinical studies to be accepted as established fact, and such abnormalities therefore must still be regarded as tentative.
Discussion, therefore, will be concentrated on those items which are relevant for an understanding of the therapeutic regimen which has been formulated with the specific intent of correcting, if possible, as many abnormalities of metabolism as possible.
Observations dating back to 1943 have demonstrated an increased rate of lipogenesis (conversion of carbohydrate into fat) in rats fed an adequate caloric diet when feeding was limited to 1 hour a day. The phenomenon has been well documented since that time by the Teppermans , by Hollifield and Parson , and by Cohn and Joseph . The latter group has found a remarkable increase in carcass fat with a fall in protein and water content in pair-fed [see definition in the paragraph below] rats as compared with normal control animals. It seems very apparent that the experimental animals had sacrificed body protein to synthesize and store fat to produce a state that has been called "non-obese obesity".
['Pair feeding' is a procedure used in medical studies to control food intake. It involves providing a control group with only as much food daily as is consumed by the experimental study group.]
Accordingly, Cohn and Joseph have concluded that a real increase in efficiency of food utilization occurs when food is eaten ... at frequent intervals. ...
[Note also that they may have concluded that by imbibing sufficient amounts of protein and water, the conversion of carbohydrates to fat may be reduced.]
Hollifield and Parson, in extending these studies, confirmed a 25-fold increase in lipogenesis [fat creation] and have demonstrated, in addition, a marked increase in synthesis of enzymes in liver and adipose [fat] tissue, of all those pathways involved in lipogenesis [fat creation], by concentrated "meal" eating in rats which normally "nibble" most of the time.
Such changes are designated technically as adaptive enzyme synthesis. They [Hollifield and Parson] further showed that this metabolic pattern could most easily be broken by imposing a 48-hour fast on the animals, after which continuous availablity of food leads to a restoration of a normal eating pattern, return to normal low level of lipogenesis [fat creation], and atrophy [withering away] of the previously hypertrophied [over-activated] enzyme systems.
Since there appear to be justifiable reasons to believe, on the basis of animal experiments, that one or two large meals eaten daily tend to promote storage of fat (obesity), the eating habits of the vast majority of obese human subjects seem almost certainly to be more than a coincidence. For most obese patients describe, spontaneously, their own efforts at weight control through dietary privation during most of the day, with food intake concentrated at one period, most often in the evening.
The "night eating syndrome" is an exaggerated form of this same pattern [eating one large meal a day rather than nibbling throughout the day]. Accordingly, it became a matter of great interest to study human metabolism in obesity by appropriate methods to determine if the same physiological principles first demonstrated in animals applied to clinical problems. Isotope studies using carbon-14-labeled glucose very quickly showed that obese subjects do not burn glucose normally, but dispose of it, instead, through increased lipogenesis [fat creation]. In this regard, as well as in many others, obese patients behave metabolically exactly like mild diabetics.
It also was possible to demonstrate that a brief fasting period changed this toward a normal pattern of glucose oxidation to carbon dioxide and water [rather than fat creation].
[A paragraph here goes into some effects of thyroid gland secretions and their analogs (similar molecules) on glucose metabolism.]
The close relationship between the metabolism of carbohydrate (glucose) and the synthesis [creation] of both fatty acids and triglyceride or neutral fat has been abundantly documented in the literature during the last few years [late 1950's, early 1960's].
In brief review, this link [between carbohydrate metabolism and creation of fatty-acids and triglycerides] is known to be mediated through three main pathways as follows:
For these reasons, and perhaps especially the last, it may be stated categorically that the storage of fat, and therefore the production and maintenance of obesity, cannot take place unless glucose is being metabolized.
... Thus an abundant supply of carbohydrate food exerts a powerful influence in directing the stream of glucose metabolism into lipogenesis [fat creation], whereas a relatively low carbohydrate intake tends to minimize storage of fat.
[There is a paragraph here on effect of palmitic acid, a polyunsaturated fatty acid, on rate of oxidation of body fat. Somewhat of a digression.]
[There are 3 paragraphs here on water retention in the obese. We go on to the "program of therapy" used for this study.]
The acutal program of therapy that has been instituted in connection with these studies is as follows:
[This is a 50-40-25 protein-fat-carb ratio --- 44%-34%-22%.
[More details of the food plan are in lists below.]
This diet is given in six feedings daily corresponding to breakfast, midmorning, lunch, midafternoon, supper, and bedtime. Every feeding is a substantial amount of food rather than a "snack".
Ideally, all feedings should be approximately the same size.
The salt content of the diet is low (between 2 and 3 gm daily). ...
The initial fast
The 48-hour fast initiates the treatment. Derived from rat experiments [described above], it is designed not to produce a spectacular loss of weight, but rather to break a metabolic pattern of augmented lipogenesis [fat creation].
During the fast, patients may have as much water, black tea, or black coffee as they wish. ... they also may be as active [or inactive] as they wish.
More on the diet
The diet has been planned around the basic concept that its carbohydrate content should be low. ...
The fat content is moderate and cannot be considered either high or low.
The total caloric value is quite high in terms of reducing diets, but its success provides excellent evidence that severe caloric restriction is not necessary for successful and even rapid weight reduction.
Careful study has indicated that the diet is adequate in every respect for adults and would also seem especially satisfactory for children and pregnant women because of its high protein content.
The multiple feedings are designed to emulate the "nibbling" pattern of rats and ruminant animals. This has been shown to minimize lipogenesis [fat creation] ...
Six feedings daily has proven to be highly acceptable to all patients and none, to date, has complained of hunger at any time. Indeed, a common complaint from most is their inability to eat so much food.
Eight or ten feedings daily would be equally satisfactory or possibly even better, if some conscientious patients wish to try such a program.
The mild salt restriction is not severe enough to make the food unpalatable, but it does tend to minimize the sodium and fluid retention problem.
One further observation should be noted. The intake of an appreciable quantity of concentrated carbohydrate food (for example, a rich dessert) regularly leads to the "binding" of a large amount of water, probably through an anti-diuretic effect that is not understood. [At least as likely: The sugars (and glucose) generated from the starches and sugars in the dessert help retain the water by an osmotic effect, similar to the way salt causes water retention.]
In a typical experimental demonstration, a severely obese man who had been losing weight very successfully on a therapeutic regiment was deliberately given an 800-gm carbohydrate, 4,000-calorie-per-day diet for 2 days, during which he gained 18 lb (8.2 kg).
Three weeks subsequently was required for his weight to return to its "precarbohydrate" level, during which time fluid balance measurements indicated marked and sustained retention. ...
Details of the Diet Plan
The diet plan is high in protein, moderate in fat, and low in carbohydrate and salt.
Six feedings daily, each containing protein, were used. The patient who so desires may eat more often than the six times a day outlined, but a minimum of six feedings is essential and should be well spaced throughout the patient's waking hours.
The diet will be outlined in detail [below]. Food condidered "free" [low in contribution to weight-gain] and foods especially contraindicated are listed first, followed by the specific foods to be eaten. Explanations are given to clarify food selections. A suggested meal pattern is given and possible changes are suggested.
"Free" Foods. - As in other reducing diets, a number of foods which are calorie-free or exceedingly low in calories are allowed in unlimited quantities. These are: noncaloric sweeteners, clear fat-free broth (Use of boullion cubes is discouraged because of their high sodum content. Instead, patients are encouraged to make their own broth, refrigerate it, and then remove the fat which hardens at the top.), unsweetened plain gelatin, artificially-sweetened gelatin products, lemon, vinegar, spices and herbs, and carbonated beverages prepared with noncaloric sweeteners.
Contraindicated Foods. - Although it should be obvious that foods not listed on the diet are not to be eaten, experience has shown it wise to specify foods especially contraindicated because of their high carbohydrate or saturated fatty acid content. These are: butter, carbonated beverages, unless prepared with a noncaloric sweetener; nuts, except for California (English) walnuts; potato chips, pretzels, crackers; sugar syrups, molasses, honey, and candy; sweetened pickles; all desserts; gelatin products sweetened with sugar; gravy and meat drippings; and alcoholic beverages.
The Daily Food Plan
1. One egg
Table for protein, fat, and carbohydrate values [grams]
|Food||Protein||Total Fat||Unsaturated Fat||Carbohydrate|
|1. One egg||6.0||6.0||---||---|
|2. 11 oz meat :|
|6 oz meat group A||42.0||26.4||3.9||---|
|5 oz meat group B||35.0||15.5||---||---|
|3. 7 servings fat :|
|4 teaspoons corn oil||---||20.0||10.0||---|
|3 teaspoons margarine||---||12.0||3.3||---|
|4. 2 cups skim milk||16.0||---||---||24|
|5. 2 servings fruit||---||---||---||20|
6. 1/2-cup B-vegetable -OR-
|7. 2 to 4 cups A-vegetable||
|Totals||101.0 gm||79.9 gm||17.2 gm||51 gm|
Source: Averages of values given in Nutritive Value of Foods,
Home and Garden Bulletin No. 72, U.S. Department of Agriculture
Note: Percent of fat that is polyunsaturated = 100 x 17.2 / 79.9 = 21.5%
Meat List - Group A
Chicken, turkey, pork (includes chops, roast, and steak)
Meat List - Group B
Fish (any kind --- canned fish should be "water packed" instead of "oil packed"), lamb (all cuts), veal (all cuts), beef (all cuts, including liver)
Discussion of meats
The meats are divided into two groups, A and B, according to their content of polyunsaturated fatty acids and total fat. Six ounces of meat or more should come from group A and 5 oz or less should come from group B. The group A meats contribute small amounts of polyunsaturated fatty acids to the diet.
Although it seems more logical to place pork in the B group of meats because of its relatively high total fat content, it was placed in the A group instead, for the following reasons:
There are good reasons for placing fish in either group A or group B. Fish was placed in group B because, in the small amounts usually eaten in the American diet, as compared with meat, it would not contribute markedly to the polyunsaturated fatty acid content of the diet.
Possible substitutions are suggested for some of the meat. Any of these substitutions alter the constituents of the diet, but are included to make the diet more realistic to follow. Substitutions suggested are:
The question of possible use of frankfurters and luncheon meats frequently arises. In general, their use is discouraged. Their relative fat content is usually higher than plain cuts of meat and the sodium content is high as well. Cereal "fillers" and dried skim milk powder frequently are added to luncheon meats. Either of these additions would increase the carbohydrate content of the diet.
|Fat||Amount in one serving|
|Corn oil, cottonseed oil, safflower oil [a]||1 teaspoon|
Mayonnaise (not more than 4 teaspoons should be used per day because of a slightly lower polyunsaturated fatty acid content and a small carbohydrate content not found in the recommended oils.)
California (English) walnuts (not more than 2 tablespoons or 10 halves should be used per day because of carbohydrate content.)
|1 tablespoon chopped or 4 to 5 halves|
Margarine made with corn oil or safflower oil (not more than 3 teaspoons should be used per day because of lower polyunsaturated fatty acid content than the recommended oils.)
The oil should not be heated to high temperatures, such as those
reached in frying, because oxidation occurs. In calculating values
for the fat list in the diet, the seven servings allowed were broken
down into 4 teaspoons of corn oil and 3 teaspoons of margarine.
Fruits may be fresh, dried, cooked, or canned, so long as no sugar is
added to them. One of the two servings of fruit allowed daily
should be a good source of ascorbic acid and are designated by an asterisk (*).
|Fruit||Amount in one serving|
|Apple (2-in. diameter)||1 small|
|Apple sauce||1/2 cup|
|Apricots, fresh||2 medium|
|Apricots, dried||4 halves|
|*Cantaloupe (6-in diameter)||1/4|
|Figs, fresh||2 large|
|Figs, dried||1 small|
|*Grapefruit juice||1/2 cup|
|Grape juice||1/4 cup|
|Honeydew melon, medium||1/8|
|*Orange juice||1/2 cup|
|Pineapple juice||1/3 cup|
|Prunes, dried||2 medium|
These vegetables are allowed either raw or cooked.
A green or yellow vegetable is recommended daily for its vitamin A content.
These vegetables, all very low in protein, fat, and
carbohydrate, are considered "free" in calculating their [body-weight
generating] values. However, since they actually do contain small
amounts of carbohydrate, an upper limit of 4 cups daily is made.
|Cauliflower||Greens [see list below]|
(Vegetable-B denotes high-carb vegetables)
Either one-half slice of bread or one-half cup of any of
the vegetables listed below can be eaten, since their protein,
fat, and carbohydrate values are so nearly the same.
Suggested Daily Meal Plan
1/2-cup vitamin C fruit or juice
1 cup skim milk
3 oz meat
2 oz meat
3 oz meat
1/2 cup skim milk
Notes on the meal plan
Ideally, the protein in the diet would be divided equally in each of the six feedings. However, a larger amount is given at the luncheon and dinner meals to more nearly resemble the American meal pattern.
The fruit, which could be eaten at any time during the day, was placed at breakfast, which is the usual meal for having a fruit high in ascorbic acid, and at dinner, so that a "dessert" can be eaten when the entire family is usually together.
Margarine is allowed at each meal, to be used on toast at breakfast and on cooked vegetables at the other two meals.
The remaining fat allowance is used as oil which can be put on salads in combination with vinegar, lemon, and spices and herbs. Other combinations of fats from the fat list also could be made. Some individuals prefer to drink the oil straight, as they would a medication.
Skim milk is suggested as the beverage between meals, since coffee or tea usually is available at meal time either at home or in a restaurant.
Women who spend their day at home have found the diet quite easy to handle. Those people working away from home must be more ingenious. Cold meat, such as leftover chicken or roast beef, can be wrapped in waxed paper and taken to work. The substitution of cheese or hard-cooked eggs can be made and may be easily slipped into a bag or purse. A meat prepared without fat or carbohydrate can be obtained in the humblest of restaurants [in the 1950's], for if no roasted, boiled, or broiled meats are available, beef patties usually are. Skim milk can be carried in a thermos bottle. Celery sticks, radishes, and raw tomatoes are good for packed lunches and are usually available in restaurants [again, in the 1950's; try to find radishes or celery in restaurants or fast food places nowadays!?! ; and tomatoes are spoiled or on the verge of spoiling about half the time, in restaurants]. Lettuce, vinegar, and oil are universally available, even if not listed on restaurant menus [again, in the 1950's; mostly salad dressing packs nowadays].
If skim milk is not available in any way during the day between meals, the following changes may be made in the diet plan:
Four eggs should be eaten each week. If a person does not want an egg every day as outlined on the diet, an ounce of meat from either group A or group B may be substituted for the egg.
For those people who find the quantity of food too large, the most advisable action to take is proportionate reduction of the amount eaten of all of the food groups. A single food or food group should not be eliminated from the diet and feedings should not be eaten less often than six times a day.
The diet, as outlined, meets 1958 recommended daily allowances of the National Research Council for adults. To retain the protein, fat, and carbohydrate values, as well as the National Research Council's recommended allowances, the only suggested change in food selection would be to reduce the fruit to one serving daily and to increase the bread to one slice daily. Other changes in food selection cannot be made which will meet the protein, fat, and carbohydrate values and still meet these recommended allowances. If a patient has known allergies or if a patient, after sincere attempts, finds the food as outlined in the diet impossible to eat, a different diet, retaining the protein, fat, and carbohydrate values, would have to be planned with nutritional supplements given to meet recommended allowances.
Clinical results that have followed the use of this plan of therapy have been remarkably encouraging and surprising.
[The reader is referred here to a graph that shows a "typical weight loss curve over a 3-month period during which 45 lb (20.4 kg) were lost. During this period the patient (female) felt no hunger." The graph shows a steady weight loss from about 229 lb to about 184 lb --- from 18 March 1963 to 24 June 1963 --- about 15 lb per month --- more than 3 lb per week.]
No patient to date has complained of hunger at any time. Some who have been especially addicted to high-carbohydrate food, particularly rich desserts, have had some "withdrawl unhappiness" for a short time, but it is not attended by hunger.
Several patients have returned to normal weight after losses of 50 to 100 lb (22.7 to 45.4 kg) and this circumstance has necessitated changes of management to maintain their improvement. The first modification has been to broaden the use of fruits and vegetables to include some which previously had not been included. These changes are additions [in calories] rather than isocaloric [same calories] substitutions. Patients are asked to do this carefully, allowing at least 2 weeks after each change before proceeding to further additions. They are next allowed increased bread, up to one slice per meal, included as additions rather than substitutions.
Throughout all these stepwise increases in food and calorie intake, they are asked to continue to divide their daily food allotment into six feedings and are again admonished that desserts should be the last additions for experimentation. Under these circumstances all patients who have evolved through this prodedure have maintained their weight loss despite increased caloric intake and have manifested no tendency to regain weight over periods of up to 6 months. Much more experience is necessary regarding this transition period before any significant conclusions can be drawn.
One of the most surprising features of this therapeutic program has been the autonomous manner in which it has operated. At the time of discharge of patients from the hospital, careful instruction is given concerning all details of treatment and they are asked merely to communicate by mail after 1 month, during which time no physician sees them. In contrast to our previous experience, very few patients thus far have failed to continue the weight loss which began in the hospital. Losses have varied from 9 to 28 lb (4.1 to 12.7 kg) during that month and have continued thereafter until the first progress visit, approximately 2 months after discharge.
In surveying this vast spectrum of metabolic changes associated with the obese state, it is mainifestly difficult or impossible to establish which abnormalities are causes and which are the effects of obesity. Likewise, we are unable to throw very much light on the baffling question of the relative importance of genetic and environmental or adaptive factors in the etiology [development] of this [obese] condition, although the former [genetics] influences are being studied   and the latter are self-evident.
We have an intuitive feeling that fasting is not the correct way to manage obesity, since it provides no opportunity for readjustment and re-education of the patient's dietary and eating habits. One unexpected dividend that has emerged from the institution of this therapeutic program has been the spontaneous evolution of new and more beneficial dietary habits in a great many patients who have commented with great surprise about the apparent loss of old compulsions to eat and modification of cravings for certain high-carbohydrate foods. [NO WONDER the doctors whose funding comes from food industries slam Atkins and his diet so unmercilessly.]
Finally, it is pertinent to ask: Is there such a clinical condition as "metabolic obesity" [obesity caused by metabolic abnormalities, rather than the other way around --- obesity causing, or being accompanied by, metabolic abnormalities]? The striking deviations from normal in most of the metabolic findings that have been described led originally to the impression that these subjects represented a separate clinical entity.
With further experience, however, the magnitude of these changes, as they are studied in patient after patient, is now seen to cover a continuous spectrum and we are more inclined to believe that "metabolic obesity" may be a stage of the obese state rather than a separate and distinct form of the condition. It appears to be more closely related to the duration than to the degree of obesity. [I suspect it can be either or both.] Only increased experience can provide the perspective necessary for a final, correct interpretation.
[If the question here is whether an abnormality in metabolism can unavoidably cause obesity, I think the concentration camps in Germany during World War II provide the answer. There were no fat prisoners in those camps after some months on their diet --- no matter what their metabolism was like. In other words, it is simple physics --- conservation of matter --- matter (fat in the body) cannot be created unless matter is introduced (to the body). And this study indicates that the kind of matter that it is important to reduce is carbohydrates (sugars and starches, rather than fiber in carbohydrates).
Reduce the amount of matter (esp. sugars and starches) going into the body, and the fat is reduced. Thus portion control and well-balanced 'real' food results in proper, healthy weight maintenance.]
In conclusion, the authors wish to reiterate that the original investigations on which this therapeutic program is based were initiated as an unbiased effort to study the perplexing and controversial problem of energy metabolism in human obesity. It is still a research project and this tentative plan of management is offered for broad trial by physicians with hope that the resulting extensive experience and further modification as new information becomes available will help to establish a final judgment of its validity.
[NOTE: Atkins simply took up the challenge issued in this last paragraph of this AMA-published paper, and, ironically, he has been villified by doctors at the highest levels of the AMA. I think that history will show that those villifying doctors have done a great dis-service to humanity --- and those doctors are actually traitors to their profession, which is supposed to promote health in their fellow citizens of the world.]
1300 University Ave., Madison 6, Wis. (Dr. Gordon)
This investigation was supported by funds from the National Institutes of Health, from Smith, Kline, and French Laboratories, and from the Wisconsin Heart Association.
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2. Gordon, E.S., and Goldberg, E.M.: Energy Metabolism in Obesity, in preparation.
3. Dole, V.P.: Relation Between Non-Esterified Fatty Acids and Metabolism of Glucose, J. Clin. Invest. 35:150, 1956.
4. Gordon, E.S.: Non-esterified Fatty Acids in Blood of Obese and Lean Subjects, Amer. J. Clin. Nutr. 8:740, 1960.
5. Opie, L.H., and Walfish, P.G.: Plasma Free Fatty Acid Concentrations in Obesity, New Eng. J. Med. 268:757, 1963.
6. Goldberg, E.M., and Gordon, E.S.: Free Fatty Acid Metabolism in Human Obesity, J. Lab. Clin. Med. 60:877, 1962.
7. Berkowitz, D.: Metabolic Changes Associated with Obesity Before and After Weight Reduction, Abstract in the Official Program of the 112th Annual Meeting of the American Medical Association, p. 89, 1963.
8. Kekwick, A.; Pawan, G.L.S.; and Chalmers, T.M.: Resistance to Ketosis in Obese Subjects, Lancet 2:1157, 1959.
9. Gordon, E.S.: Unpublished observations.
10. Bansi, H.W. and Olsen, J.M.: Water Retention in Obesity, Acta Endocr. 32:113, 1959.
11. Elsback, P. and Schwartz, I.L.: Salt and Water Metabolism During Weight Reduction, Metabolism 10:595, 1961.
12. Roth, J. et al: Secretion of Human Growth Hormone: Physiologic and Experimental Modification, Metabolism 12:577, 1963.
13. Schteingart, D.E.; Gregerman, R.I.; and Conn, J.W.: Comparison of Characteristics of Increased Adrenocortical Function in Obesity and Cushing's Syndrome, Metabolism 12:484, 1963.
14. Randle, P.J., et al: Glucose Fatty Acid Cycle, Lancet 1:785, 1963.
15. Hales, C.N., and Randle, P.J.: Effects of Low Carbohydrate Diet and Diabetes Mellitus on Plasma Concentrations of Glucose, Non-Esterified Fatty Acid and Insulin During Oral Glucose Tolerance Tests, Lancet 1:790, 1963.
16. Grodsky, G.M., et al: Reduction by Phenformin of Excessive Insulin Levels After Glucose Loading in OBese and Diabetic Subjects, Metabolism 12:278, 1963.
17. Stuchlikova, E., et al: Some Changes in Intermediary Metabolism of Obese Patients, Clin. Chim. Acta 6:571, 1961.
18. Dickerson, V.C.; Tepperman, J.; and Long, C.N.H.: Role of Liver in Synthesis of Fatty Acids from Carbohydrate, Yale J. Biol. Med. 15:875, 1943.
19. Tepperman, J., and Tepperman, H.M.: Effects of Antecedent Food Intake Pattern on Hepatic Lipogenesis, Amer. J. Physiol. 193:55, 1958.
20. Hollifield, G., and Parson, W.: Metabolic Adaptations to "Stuff and Starve" Program: I. Studies of Adipose Tissue and Liver Glycogen in Rats Limited to Short Daily Feeding Period, J. Clin. Invest. 41:245, 1962.
21. Cohn, C., and Joseph, D.: Effects on Metabolism Produced by Rate of Ingestion of Diet, Amer. J. Clin. Nutr. 8:682, 1960.
22. Cohn, C., and Joseph, D.: Influence of Body Weight and Body Fat on Appetite of "Normal" Lean and Obese Rats, Yale J. Biol. Med. 34:598, 1962.
23. Bedell, G.N.; Wilson, W.R.; and Seebohm, P.M.: Pulmonary Function in Obese Persons, J. Clin. Invest. 37:1049, 1958.
24. Doorenbos, H.; Cost, W.S.; and Nagelsmit, W.F.: Effect of Aldosterone Antagonists on Disturbance of Carbohydrate Metabolism in Primary Aldoteronism, Acta Endocr., suppl. 51, Abstracts, No. 93, p. 185.
25. Steinberg, A.G.: Comments on Genetics of Human Obesity, Amer. J. Clin. Nutr. 8:752, 1960.
26. Astwood, E.B.: Heritage of Corulence, Endocrinology 71:337, 1962.
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This blog content was posted 2008 Jan 29.